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目的 :观察核因子κB(NF-κB)水平在大鼠血液高凝态下的变化,为血栓疾病的防治探索新靶点。方法 :大鼠80只随机分为模型组与生理盐水组,模型组以预实验确定的最适剂量盐酸肾上腺素造模,于12、18、24、48、96 h各组随机取8只大鼠颈动脉取血测凝血酶原时间(PT)、活化部分凝血活酶时间(APTT)、全血黏度,并采用酶联免疫吸附法测NF-κB水平。结果:0.7 mg/kg肾上腺素造模组模型复制成功率高,大鼠死亡率低,为最佳造模剂量。生理盐水组PT、APTT、全血黏度及NF-κB水平在各时间点无统计学差异;模型组PT、APTT较生理盐水组缩短(P<0.05),但随时间缓慢延长,全血黏度及NF-κB水平较生理盐水组增大(P<0.05),但随时间缓慢降低,且在12、18 h时PT、APTT同生理盐水组比较有显著差异(P<0.05),24 h内全血黏度较生理盐水组显著增大(P<0.05),48 h内NF-κB水平较生理盐水组显著升高(P<0.05)。结论:高凝态大鼠血液中NF-κB水平显著升高,并随着高凝态的消退而降低,说明大鼠血液高凝态的发生、发展可能与NF-κB信号通路表达上调有关。
Objective: To observe the changes of NF-κB in blood hypercoagulable state in rats and to explore new targets for the prevention and treatment of thrombus diseases. Methods: Eighty rats were randomly divided into model group and normal saline group. The model group was established with the best dose of adrenaline hydrochloride preconditioned. At 12,18,24,48 and 96 h, 8 rats Blood samples were taken from the carotid artery to measure PT, activated partial thromboplastin time (APTT) and whole blood viscosity, and the level of NF-κB was measured by enzyme-linked immunosorbent assay. Results: The success rate of 0.7 mg / kg adrenaline model group was high, and the mortality rate of rats was low, which was the best model dose. Compared with normal saline group, PT, APTT, whole blood viscosity and NF-κB in normal saline group had no significant difference at each time point. PT and APTT in model group were shorter than those in normal saline group (P <0.05) The level of NF-κB was increased (P <0.05), but decreased slowly with time. Compared with saline group, the levels of NF-κB and APTT at 12, 18 h were significantly different (P <0.05) Compared with saline group, the blood viscosity increased significantly (P <0.05), and the level of NF-κB increased significantly (P <0.05) compared with saline group within 48 h. CONCLUSION: NF-|ÊB levels in the blood of hypercoagulable rats are significantly increased and decrease with hypercoagulability, indicating that hypercoagulability in blood may be related to the upregulation of NF-|ÊB signaling pathway.